The cerebral endothelium during pregnancy: A potential role in the development of eclampsia

被引:8
作者
Cipolla, MJ
Vitullo, L
DeLance, N
Hammer, E
机构
[1] Univ Vermont, Coll Med, Dept Neurol, Burlington, VT 05405 USA
[2] Univ Vermont, Coll Med, Dept Pharmacol, Burlington, VT 05405 USA
[3] Univ Vermont, Coll Med, Dept Obstet Gynecol, Burlington, VT 05405 USA
来源
ENDOTHELIUM-JOURNAL OF ENDOTHELIAL CELL RESEARCH | 2005年 / 12卷 / 1-2期
关键词
acute hypertension; blood-brain barrier; cerebral endothelium; pregnancy;
D O I
10.1080/10623320590933725
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The authors investigated the influence of pregnancy on cerebral endothelial cell permeability in response to an acute elevation in intravascular pressure that caused forced dilatation of myogenic tone. Third-order branches of the posterior cerebral artery (PCA). were dissected from nonpregnant (NP) and late-pregnant (LP, days 19 to 20) Sprague-Dawley rats and mounted on glass cannulas in an arteriograph chamber that allowed control over intravascular pressure and measurement of both diameter and permeability to fluorescent dextran (3000 Da). Permeability was determined at 75 mm Hg and after a step increase in pressure to 200 mm Hg. The extent of pinocytosis and transcellular transport in response to pressure was evaluated separately in the same groups of animals at 75 and 200 mm Hg using transmission electron microscopy. All arteries developed myogenic tone at 75 mm Hg that was lost when pressure was increased to 200 mm Hg to cause forced dilatation. The increased pressure caused a significant increase in permeability to dextran and enhanced pinocytosis in arteries from LP animals, but not in NP animals whose permeability remained constant at both pressures. These results suggest a pregnancy-specific effect on the cerebral endothelium that may promote enhanced vascular permeability during acute hypertension and may contribute to the edema formation and neurologic complications of eclampsia.
引用
收藏
页码:5 / 9
页数:5
相关论文
共 20 条
[1]  
BARRON WM, 1991, MED DISORDERS PREGNA, P1
[2]  
BETZ AL, 1998, CEREBROVASC DIS, V1, pCH25
[3]   Cerebral artery reactivity changes during pregnancy and the postpartum period: a role in eclampsia? [J].
Cipolla, MJ ;
Vitullo, L ;
McKinnon, J .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2004, 286 (06) :H2127-H2132
[4]   Transcellular transport as a mechanism of blood-brain barrier disruption during stroke [J].
Cipolla, MJ ;
Crete, R ;
Vitullo, L ;
Rix, RD .
FRONTIERS IN BIOSCIENCE-LANDMARK, 2004, 9 :777-785
[5]  
DINSDALE HB, 1998, STROKE PATHOPHYSIOLO, pCH34
[6]   THE BRAIN IN ECLAMPSIA [J].
DONALDSON, JO .
HYPERTENSION IN PREGNANCY, 1994, 13 (02) :115-133
[7]   Assessment of vasogenic edema in eclampsia using diffusion imaging [J].
Engelter, ST ;
Provenzale, JM ;
Petrella, JR .
NEURORADIOLOGY, 2000, 42 (11) :818-820
[8]   INDUCTION OF PINOCYTOSIS IN CEREBRAL VESSELS BY ACUTE HYPERTENSION AND BY HYPER-OSMOLAR SOLUTIONS [J].
HANSSON, HA ;
JOHANSSON, BB .
JOURNAL OF NEUROSCIENCE RESEARCH, 1980, 5 (03) :183-190
[9]   ULTRASTRUCTURAL STUDIES ON CEREBROVASCULAR PERMEABILITY IN ACUTE HYPERTENSION [J].
HANSSON, HA ;
JOHANSSON, B ;
BLOMSTRAND, C .
ACTA NEUROPATHOLOGICA, 1975, 32 (03) :187-198
[10]  
Manfredi M, 1997, ACTA NEUROL SCAND, V96, P277